Database : MEDLINE
Search on : Neurotoxicity and Syndromes [Words]
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[PMID]: 29446298
[Au] Autor:Katamanova EV; Dyakovich MP; Kudaeva IV; Shevchenko OI; Eshchina IM; Rukavishnikov VS; Meshchakova NM
[Ti] Title:[Clinical and neurophysiological peculiarities of health disorders in workers in dependence on the vinyl chloride exposure load].
[So] Source:Gig Sanit;95(12):1167-71, 2016.
[Is] ISSN:0016-9900
[Cp] Country of publication:Russia (Federation)
[La] Language:rus
[Ab] Abstract:Results of the clinical and neurophysiological examinations of 42 workers with operating history at the chemical plant exposed to vinyl chloride (VC) are presented. The purpose of research was the identification ofpeculiarities of clinical manifestations and disorders of the functional activity of the brain in workers at the vinyl chloride production, with taking into account the exposure toxic load (ETL). There were made clinical and electroencephalographic examinations with the detection of cognitive evoked potentials (CEP) and statistical analysis of results with the use of the Mann-Whitney U-test, Fisher's F-test, calculation of Spearman's correlation coefficient. The features in clinical picture of the pathology of the nervous system were detected in the form of asthenic disorders with cognitive impairment and autonomic dysfunction syndrome. There was established the increase in the cognitive impairment rate (p = 0.03), the decline in a-EEG activity (p = 0.01) and the worsening of indices of the amplitude (p = 0.011) and latency (p = 0,05) of CEP in extremely high level of ETL in comparison with same indices in the group with moderately high ETL. In the first group there was revealed a statistically significant exceedance of the frequency of hypertension - by 1.6 times, skin diseases - by 9 times, chronic subatrophic rhino-pharyngitis by 1.4 times in comparison with cases from the second group. In the group with moderately high level of ETL there was established the statistically significant inverse correlationship between the ETL and the index of P300 amplitude from the left side (r = -0.38, p = 0.019) and in the group with extremely high level ETL - between ETL and index of the ß2 - rhythm (r = - 0.73, p = 0.0008).
[Mh] MeSH terms primary: Air Pollutants, Occupational
Manufacturing Industry
Neurotoxicity Syndromes
Vinyl Chloride
[Mh] MeSH terms secundary: Air Pollutants, Occupational/analysis
Air Pollutants, Occupational/toxicity
Electroencephalography/methods
Humans
Male
Manufacturing Industry/methods
Manufacturing Industry/standards
Middle Aged
Neurotoxicity Syndromes/diagnosis
Neurotoxicity Syndromes/epidemiology
Neurotoxicity Syndromes/etiology
Neurotoxicity Syndromes/physiopathology
Occupational Exposure/adverse effects
Occupational Exposure/analysis
Occupational Exposure/prevention & control
Risk Assessment/methods
Risk Assessment/statistics & numerical data
Risk Factors
Siberia/epidemiology
Time Factors
Vinyl Chloride/analysis
Vinyl Chloride/toxicity
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Air Pollutants, Occupational); WD06X94M2D (Vinyl Chloride)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180216
[St] Status:MEDLINE

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[PMID]: 29446282
[Au] Autor:Bodienkova GM; Rukavishnikov VS; Boklazhenko EV
[Ti] Title:[The evaluation of immunoregulatory markers in the course of neurointoxication by mercury over the post-exposure period].
[So] Source:Gig Sanit;95(12):1138-41, 2016.
[Is] ISSN:0016-9900
[Cp] Country of publication:Russia (Federation)
[La] Language:rus
[Ab] Abstract:There was executed the examination of patients with occupational chronic mercury intoxication in the post-exposure period after the exposure to metallic mercury vapor. 47 persons with an established diagnosis of chronic mercury intoxication (HMI) passed the laboratory and immunological examination in the period of exposure to metallic mercury vapor in a production environment. The average age of men accounted for 49.2±1.2 years. The experience of work in hazardous working conditions amounted of 21.65±1.61 years (1 observation). All these same cases were observed in the institute clinic again after 5 years (2 observation) and 10 years (3 observation). A control group of healthy men consisted of 47 cases included persons of representative both age and general work experience, without a professional route of contact with hazardous substances. The level of such cytokines as IL-1ß, IL-2, IL-4, IL-6, TNF-a, INF-y and neurotropic IgG class antibodies directed to proteins of the nervous tissue (NF-200, GFAP, MBP, B-dependent Ca-channel, Glu-R, DA-R, R-GABA, Ser-R, R-Chol, DNA, B2GP) in serum were determined by enzyme linked immunosorbent assay. There was established the gain in the imbalance of inflammatory mediators and production ofneural antibodies in dynamics after the termination of the production in conditions of metallic mercury vapors. Revealed features of the regulatory relationship between the level of cytokines and the severity of the autoimmune process were shown to contribute to the maintenance and progression of neurodegenerative processes. There was recommended the identification of immunoregulatory markers (IL-1ß, IL-4, TNF-a, NF-AT to 200, GFAP, S-100) as an additional criteria for the diagnosis of health disorders in operating and monitoring the course of the progredient professional mercury intoxication.
[Mh] MeSH terms primary: Cytokines
Mercury Poisoning, Nervous System
Mercury
Occupational Diseases
[Mh] MeSH terms secundary: Antibody Formation/drug effects
Biomarkers/analysis
Biomarkers/blood
Chemical Industry/methods
Chemical Industry/standards
Cytokines/analysis
Cytokines/blood
Follow-Up Studies
Humans
Male
Mercury/immunology
Mercury/toxicity
Mercury Poisoning, Nervous System/diagnosis
Mercury Poisoning, Nervous System/immunology
Mercury Poisoning, Nervous System/prevention & control
Middle Aged
Occupational Diseases/diagnosis
Occupational Diseases/etiology
Occupational Diseases/immunology
Occupational Diseases/prevention & control
Occupational Health/standards
Occupational Health/statistics & numerical data
Siberia/epidemiology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Biomarkers); 0 (Cytokines); FXS1BY2PGL (Mercury)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180216
[St] Status:MEDLINE

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[PMID]: 28822947
[Au] Autor:Zong L; Xing J; Liu S; Liu Z; Song F
[Ad] Address:National Center of Mass Spectrometry in Changchun, Jilin Province Key Laboratory of Chinese Medicine Chemistry and Mass Spectrometry, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun 130022, China; University of Chinese Academy of Sciences, Beijing 100039, China.
[Ti] Title:Cell metabolomics reveals the neurotoxicity mechanism of cadmium in PC12 cells.
[So] Source:Ecotoxicol Environ Saf;147:26-33, 2018 Jan.
[Is] ISSN:1090-2414
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The heavy metals such as cadmium (Cd) can induce neurotoxicity. Extensive studies about the effects of Cd on human health have been reported, however, a systematic investigation on the molecular mechanisms of the effects of Cd on central nervous system is still needed. In this paper, the neuronal PC-12 cells were treated with a series of concentrations of CdCl for 48h. Then the cytotoxicity was evaluated by MTT (3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide) assay. The IC value (15% inhibiting concentration) was selected for further mechanism studies. After PC-12 cells incubated with CdCl at a dose of IC for 48h, the intracellular and extracellular metabolites were profiled using ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS)-based cell metabolomics approach. As found, the effects of the heavy metal Cd produced on the PC-12 cell viability were dose-dependent. The metabolic changes were involved in the glycolysis and gluconeogenesis, biopterin metabolism, tryptophan metabolism, tyrosine metabolism, glycerophospholipid metabolism, and fatty acids beta-oxidation. These could cause the perturbation of cell membrane, redox balance, energy supply, cellular detoxification, further affecting the cellular proliferation and apoptosis and other cellular activities.
[Mh] MeSH terms primary: Cadmium/toxicity
Environmental Pollutants/toxicity
Metabolome/drug effects
Metabolomics/methods
Neurons/drug effects
Neurotoxicity Syndromes/metabolism
[Mh] MeSH terms secundary: Animals
Biomarkers/metabolism
Cell Survival/drug effects
Energy Metabolism/drug effects
Humans
Neurons/metabolism
Neurons/pathology
Oxidation-Reduction
PC12 Cells
Rats
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Biomarkers); 0 (Environmental Pollutants); 00BH33GNGH (Cadmium)
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:170821
[St] Status:MEDLINE

  4 / 10521 MEDLINE  
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[PMID]: 28452906
[Au] Autor:Hsu CW; Lee Y; Lee CY; Lin PY
[Ad] Address:Department of Psychiatry, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
[Ti] Title:Reversible Pisa Syndrome Induced by Rivastigmine in a Patient With Early-Onset Alzheimer Disease.
[So] Source:Clin Neuropharmacol;40(3):147-148, 2017 May/Jun.
[Is] ISSN:1537-162X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Pisa syndrome (PS) is a state of dystonic muscle contraction with a marked truncal deviation to one side. It is an uncommon adverse effect of antipsychotic drugs, but is rarely reported in patients receiving acetylcholinesterase inhibitors, especially rivastigmine. We present a 57-year-old female patient with Alzheimer disease who began to develop symptoms of dementia at the age of 51 years. She was observed to have symptoms of PS after continuous use of rivastigmine (9 mg/d) for nearly 2 years. The PS symptoms improved after the dose of rivastigmine was reduced but recurred when the dose was added back to 9 mg/d. Finally, after we decreased the dose to 4.5 mg/d, her PS symptoms were remitted. This report reminds us that clinicians need to be cautious about the risk of PS when prescribing rivastigmine in a patient with early-onset Alzheimer disease.
[Mh] MeSH terms primary: Alzheimer Disease/drug therapy
Cholinesterase Inhibitors/adverse effects
Neuroprotective Agents/adverse effects
Neurotoxicity Syndromes/therapy
Rivastigmine/adverse effects
[Mh] MeSH terms secundary: Cholinesterase Inhibitors/administration & dosage
Cholinesterase Inhibitors/therapeutic use
Dose-Response Relationship, Drug
Drug Monitoring
Dystonic Disorders/etiology
Dystonic Disorders/prevention & control
Female
Humans
Middle Aged
Neuroimaging
Neuroprotective Agents/administration & dosage
Neuroprotective Agents/therapeutic use
Neurotoxicity Syndromes/diagnostic imaging
Neurotoxicity Syndromes/physiopathology
Rivastigmine/administration & dosage
Rivastigmine/therapeutic use
Treatment Outcome
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Nm] Name of substance:0 (Cholinesterase Inhibitors); 0 (Neuroprotective Agents); PKI06M3IW0 (Rivastigmine)
[Em] Entry month:1803
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[Js] Journal subset:IM
[Da] Date of entry for processing:170429
[St] Status:MEDLINE
[do] DOI:10.1097/WNF.0000000000000215

  5 / 10521 MEDLINE  
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[PMID]: 29442005
[Au] Autor:Petroianu GA
[Ti] Title:Neuropathic organophosphates: from Scrugham, Heim and Lorot to Jake leg paralysis.
[So] Source:Pharmazie;71(12):738-744, 2016 Dec 01.
[Is] ISSN:0031-7144
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Henry Scrugham (1811-1898), the father of triphenyl-phosphate, was a student of Alexander Williamson (1824-1904), Professor of analytical and practical chemistry at the University College London. Williamson using the approach perfected by Scurgham reacted phosphorus pentachloride with cresol (a mixture of ortho, para and meta isomers) thus obtaining tricresyl phosphate (TCP). The triesters of phenol, cresol and naphtol were prepared with a higher yield by Rudolf Heim (1861-1919) by their respective reaction with phosphorus oxychloride (POCl3). Heim is also the first one to obtain pure tri-o-cresyl phosphate (TOCP). In the meantime French pharmacist Jules Brissonnet (1859-1915) synthesized creosote phosphate (containing i.a. TOCP) and popularized its use in the treatment of pulmonary phthisis (tuberculosis). Camille Lorot (1872-1951) and others in France and Germany recognized the ability of creosote phosphate to induce polyneuropathies but this knowledge did not prevent the Ginger Jake epidemic (Jake leg) of the 1930s in the US. The Jake induced neuropathy was first recognized and described in Oklahoma City by a General Practitioner, Ephraim Goldfain (1894-1983). Soon thereafter Maurice Isadore Smith (1887-1951), a pharmacologist, and chemist Elias Elvove (1883-1962) identified TOCP in Jamaican ginger extract as the causative agent. We attempt to shed some light on the life and family of the less known chemists, pharmacists and physicians associated with the synthesis of neuropathic organophosphates and with the recognition of their toxicity.
[Mh] MeSH terms primary: Neurotoxicity Syndromes/history
Organophosphates/toxicity
[Mh] MeSH terms secundary: History, 19th Century
History, 20th Century
Neurotoxicity Syndromes/pathology
Organophosphates/chemical synthesis
[Pt] Publication type:BIOGRAPHY; HISTORICAL ARTICLE; JOURNAL ARTICLE; PORTRAITS
[Ps] Personal name as subject:Scrugham H; Heim R; Brissonnet J; Goldfain E; Elvove E; Smith M
[Nm] Name of substance:0 (Organophosphates)
[Em] Entry month:1802
[Cu] Class update date: 180227
[Lr] Last revision date:180227
[Js] Journal subset:IM
[Da] Date of entry for processing:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6080

  6 / 10521 MEDLINE  
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[PMID]: 29471776
[Au] Autor:Sharpe ME
[Ad] Address:Cell and Gene Therapy Catapult, Guy's Hospital, Great Maze Pond, London, United Kingdom.
[Ti] Title:T-cell Immunotherapies and the Role of Nonclinical Assessment: The Balance between Efficacy and Pathology.
[So] Source:Toxicol Pathol;46(2):131-146, 2018 Feb.
[Is] ISSN:1533-1601
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Gene-engineered T-cell therapies have the potential to revolutionize the treatment of cancer. These therapies have shown exceptional clinical efficacy specifically in the field of B-cell malignancies and the first products (Kymriah™ and Yescarta™) have recently been approved in the United States for specific indications. The power of these treatments is also linked with a distinct set of toxicities both predicted and unpredicted, including off-tumor activity, cytokine release syndromes, and neurotoxicity, occasionally with fatal consequences. As these therapies begin to reach more patients, it is critical to develop the nonclinical tools to adequately determine the mechanisms driving these toxicities, to assess the safety risks of candidate products, and to develop strategies for safety management.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180223
[Lr] Last revision date:180223
[St] Status:In-Data-Review
[do] DOI:10.1177/0192623317752101

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[PMID]: 29413859
[Au] Autor:Guo P; Liu A; Huang D; Wu Q; Fatima Z; Tao Y; Cheng G; Wang X; Yuan Z
[Ad] Address:National Reference Laboratory of Veterinary Drug Residues (HZAU) and MAO Key Laboratory for Detection of Veterinary Drug Residues, Wuhan, China.
[Ti] Title:Brain damage and neurological symptoms induced by T-2 toxin in rat brain.
[So] Source:Toxicol Lett;286:96-107, 2018 Apr.
[Is] ISSN:1879-3169
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:T-2 toxin, a trichothecene mycotoxin, is a common contaminant in food and animal feed, and is also present in processed cereal products. The most common route of T-2 toxin exposure in humans is through dietary ingestion. The cytotoxic effects of T-2 toxin include modifications to feeding behavior, nervous disorders, cardiovascular alterations, immunosuppression, and hemostatic derangements. However, to date, effects on the central nervous system (CNS) have rarely been reported. In the present study, female Wistar rat were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at one, three, and seven days post-exposure. Histopathological analysis and transmission electron microscope (TEM) observations were used to investigate injury to the brain and pituitary gland. Damage to the brain and pituitary at the molecular level was detected by real time-polymerase chain reaction (RT-PCR), western blot, and immunohistochemical assays. Liquid chromatograph-mass spectrometer/mass spectrometer (LC-MS/MS) was used to investigate T-2 concentration in the brain. The results showed that pathological lesions were obvious in the brain at three days post-exposure; lesions in the pituitary were not observed until seven days post-exposure. Autophagy in the brain and apoptosis in the pituitary suggest that T-2 toxin may induce different acute reactions in different tissues. Importantly, low concentrations of T-2 toxin in the brain were observed in only one rat. Responsible for the above mentioned, we hypothesize that brain damage caused by this toxin may be due to the ability of the toxin to directly cross the blood-brain barrier (BBB). Therefore, given its widespread pollution in food, we should pay more attention to the neurotoxic effects of the T-2 toxin, which may have widespread implications for human health.
[Mh] MeSH terms primary: Brain/drug effects
Neurotoxicity Syndromes/etiology
T-2 Toxin/toxicity
[Mh] MeSH terms secundary: Animals
Apoptosis/drug effects
Autophagy/drug effects
Behavior, Animal/drug effects
Blood-Brain Barrier/metabolism
Blotting, Western
Brain/metabolism
Brain/ultrastructure
Capillary Permeability
Chromatography, Liquid
Female
Gene Expression Regulation
Immunohistochemistry
Microscopy, Electron, Transmission
Neurotoxicity Syndromes/metabolism
Neurotoxicity Syndromes/pathology
Neurotoxicity Syndromes/psychology
Pituitary Gland/drug effects
Pituitary Gland/metabolism
Pituitary Gland/ultrastructure
Rats, Wistar
Real-Time Polymerase Chain Reaction
Risk Assessment
T-2 Toxin/metabolism
Tandem Mass Spectrometry
Time Factors
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:I3FL5NM3MO (T-2 Toxin)
[Em] Entry month:1802
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[Js] Journal subset:IM
[Da] Date of entry for processing:180208
[St] Status:MEDLINE

  8 / 10521 MEDLINE  
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[PMID]: 29258821
[Au] Autor:Masuda K; Tsutsuki H; Kasamatsu S; Ida T; Takata T; Sugiura K; Nishida M; Watanabe Y; Sawa T; Akaike T; Ihara H
[Ad] Address:Department of Biological Science, Graduate School of Science, Osaka Prefecture University, Osaka, Japan; Project Management Department, SHIONOGI & CO., LTD., Osaka, Japan.
[Ti] Title:Involvement of nitric oxide/reactive oxygen species signaling via 8-nitro-cGMP formation in 1-methyl-4-phenylpyridinium ion-induced neurotoxicity in PC12 cells and rat cerebellar granule neurons.
[So] Source:Biochem Biophys Res Commun;495(3):2165-2170, 2018 01 15.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:To investigate the role of nitric oxide (NO)/reactive oxygen species (ROS) redox signaling in Parkinson's disease-like neurotoxicity, we used 1-methyl-4-phenylpyridinium (MPP ) treatment (a model of Parkinson's disease). We show that MPP -induced neurotoxicity was dependent on ROS from neuronal NO synthase (nNOS) in nNOS-expressing PC12 cells (NPC12 cells) and rat cerebellar granule neurons (CGNs). Following MPP treatment, we found production of 8-nitroguanosine 3',5'-cyclic monophosphate (8-nitro-cGMP), a second messenger in the NO/ROS redox signaling pathway, in NPC12 cells and rat CGNs, that subsequently induced S-guanylation and activation of H-Ras. Additionally, following MPP treatment, extracellular signal-related kinase (ERK) phosphorylation was enhanced. Treatment with a mitogen-activated protein kinase (MAPK)/ERK kinase (MEK) inhibitor attenuated MPP -induced ERK phosphorylation and neurotoxicity. In conclusion, we demonstrate for the first time that NO/ROS redox signaling via 8-nitro-cGMP is involved in MPP -induced neurotoxicity and that 8-nitro-cGMP activates H-Ras/ERK signaling. Our results indicate a novel mechanism underlying MPP -induced neurotoxicity, and therefore contribute novel insights to the mechanisms underlying Parkinson's disease.
[Mh] MeSH terms primary: 1-Methyl-4-phenylpyridinium
Cerebellum/metabolism
Cyclic GMP/analogs & derivatives
Neurons/metabolism
Nitric Oxide/metabolism
Parkinsonian Disorders/metabolism
Reactive Oxygen Species/metabolism
[Mh] MeSH terms secundary: Animals
Cells, Cultured
Cerebellum/drug effects
Cerebellum/pathology
Cyclic GMP/metabolism
Dose-Response Relationship, Drug
Neurons/drug effects
Neurons/pathology
Neurotoxins
PC12 Cells
Parkinsonian Disorders/chemically induced
Rats
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (8-nitroguanosine 3',5'-cyclic monophosphate); 0 (Neurotoxins); 0 (Reactive Oxygen Species); 31C4KY9ESH (Nitric Oxide); H2D2X058MU (Cyclic GMP); R865A5OY8J (1-Methyl-4-phenylpyridinium)
[Em] Entry month:1802
[Cu] Class update date: 180213
[Lr] Last revision date:180213
[Js] Journal subset:IM
[Da] Date of entry for processing:171221
[St] Status:MEDLINE

  9 / 10521 MEDLINE  
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[PMID]: 29191454
[Au] Autor:Kraemer ÂB; Parfitt GM; Acosta DDS; Bruch GE; Cordeiro MF; Marins LF; Ventura-Lima J; Monserrat JM; Barros DM
[Ad] Address:Programa de Pós-Graduação em Ciências Fisiológicas, Universidade Federal do Rio Grande - FURG, Rio Grande, RS, Brazil.
[Ti] Title:Fullerene (C60) particle size implications in neurotoxicity following infusion into the hippocampi of Wistar rats.
[So] Source:Toxicol Appl Pharmacol;338:197-203, 2018 01 01.
[Is] ISSN:1096-0333
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The buckminsterfullerene (C60) is considered as a relevant candidate for drug and gene delivery to the brain, once it has the ability to cross the blood-brain barrier. However, the biological implications of this nanomaterial are not fully understood, and its safety for intracerebral delivery is still debatable. In this study, we investigated if C60 particle size could alter its biological effects. For this, two aqueous C60 suspensions were used with maximum particle size up to 200nm and 450nm. The suspensions were injected in the hippocampus, the main brain structure involved in memory processing and spatial localization. In order to assess spatial learning, male Wistar rats were tested in Morris water maze, and the hippocampal BDNF protein levels and gene expression were analyzed. Animals treated with C60 up to 450nm demonstrated impaired spatial memory with a significant decrease in BDNF protein levels and gene expression. However, an enhanced antioxidant capacity was observed in both C60 treatments. A decrease in reactive oxygen species levels was observed in the treatments with suspensions containing particles measuring with up to 450nm. Thiobarbituric acid reactive substances, glutamate cysteine ligase, and glutathione levels showed no alterations among the different treatments. In conclusion, different particle sizes of the same nanomaterial can lead to different behavioral outcomes and biochemical parameters in brain tissue.
[Mh] MeSH terms primary: Fullerenes/toxicity
Hippocampus/drug effects
Neurotoxicity Syndromes/etiology
[Mh] MeSH terms secundary: Animals
Brain-Derived Neurotrophic Factor/analysis
Hippocampus/metabolism
Male
Particle Size
Rats
Rats, Wistar
Reactive Oxygen Species/metabolism
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Brain-Derived Neurotrophic Factor); 0 (Fullerenes); 0 (Reactive Oxygen Species)
[Em] Entry month:1801
[Cu] Class update date: 180213
[Lr] Last revision date:180213
[Js] Journal subset:IM
[Da] Date of entry for processing:171202
[St] Status:MEDLINE

  10 / 10521 MEDLINE  
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[PMID]: 29328996
[Au] Autor:Millan NC; Pastrana A; Guitter MR; Zubizarreta PA; Monges MS; Felice MS
[Ad] Address:Hematology and Oncology Department, Hospital de Pediatría Prof. Dr. Juan P. Garrahan, Buenos Aires, Argentina. Electronic address: naty_millan@yahoo.com.ar.
[Ti] Title:Acute and sub-acute neurological toxicity in children treated for acute lymphoblastic leukemia.
[So] Source:Leuk Res;65:86-93, 2018 Feb.
[Is] ISSN:1873-5835
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Eighty percent of children with acute lymphoblastic leukemia (ALL) survive with current treatments. Neurotoxicity is an infrequent adverse event. We describe clinical presentations of neurological toxicity, phases of treatment when these adverse events were more frequent and patients ́ outcome. From January-1995 to December-2015, 1379 ALL cases were admitted. Neurotoxicity was diagnosed in 49 patients (3.6%) and classified according to neurological syndromes. Medical records, laboratory-tests and images were reviewed. The diagnosed syndromes were: a) Methotrexate-leukoencephalopathy (MLE) (35.4%); b) Cerebral-venous-sinus thrombosis following L-Asparaginase administration (26.5%); c) Vincristine-induced-vocal-cord paralysis (VVCP) (14.2%); d) Stroke-associated vasospasm (14%), after high-dose methotrexate e) Severe polyneuropathy (6.1%); f) Methotrexate myelopathy (2%); and g) Pseudotumor-cerebri (2%) associated with corticosteroid therapy. Neurotoxicity was diagnosed during induction in 55% of cases. We conclude that MLE was the most frequent syndrome. VVCP was observed in infants and Down patients. Seizure was the most common symptom and toxicity occurred mainly during induction phase.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1801
[Cu] Class update date: 180206
[Lr] Last revision date:180206
[St] Status:In-Data-Review


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